Neuronal reperfusion damage after forebrain ischemia in rats at different intervals
Yusheng Sun
Abstract
Yusheng Sun
Abstract
Aim: To observe the damage of hippocampus, striatum, and cortical neurons after transient forebrain ischemia in the rats.Methods: Cerebral ischemic models were made by clamping bilateral carotid arteries for 5 min. Neuronal damage was studied by electric microscope and sequential Tunel technique. Results: On the 2nd day after the transient forebrain ischemia, neuronal necrosis and apoptosis in striatum and cotrex were serious. On the 4th day, neuronal necrosis in hippocampus was slight, but neuronal apoptosis was serious. The dyeing of Tunel indicated that the typical apoptosis remained for a short time. The colors of neuronal apoptosis were different. The number of necrotic neurons did not increase from the 2nd day after ischemia. Conclusions: Cerebral ischemia can cause neuronal necrosis and apoptosis. The lasting time for apoptosis is short. After that, the morphological change of neurons is similar to necrosis, and the ability of anti ischemia in different cerebral parts is greatly different.
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Aim: To observe the damage of hippocampus, striatum, and cortical neurons after transient forebrain ischemia in the rats.Methods: Cerebral ischemic models were made by clamping bilateral carotid arteries for 5 min. Neuronal damage was studied by electric microscope and sequential Tunel technique. Results: On the 2nd day after the transient forebrain ischemia, neuronal necrosis and apoptosis in striatum and cotrex were serious. On the 4th day, neuronal necrosis in hippocampus was slight, but neuronal apoptosis was serious. The dyeing of Tunel indicated that the typical apoptosis remained for a short time. The colors of neuronal apoptosis were different. The number of necrotic neurons did not increase from the 2nd day after ischemia. Conclusions: Cerebral ischemia can cause neuronal necrosis and apoptosis. The lasting time for apoptosis is short. After that, the morphological change of neurons is similar to necrosis, and the ability of anti ischemia in different cerebral parts is greatly different.
Key concepts: Ischemia, Necrosis, TUNEL assay, Hippocampus, Apoptosis, Forebrain, Striatum, Neuroscience